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The inhibitory effect of Ramalin on the expression of VCAM‐1 in human aortic smooth muscle cells
Author(s) -
Park Bongkyun,
Rhee Dong-kwon,
Pyo Suhkneung
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb369
Subject(s) - vcam 1 , cell adhesion molecule , cell adhesion , inflammation , chemistry , tumor necrosis factor alpha , adhesion , vascular smooth muscle , microbiology and biotechnology , phosphorylation , signal transduction , nf κb , pharmacology , cancer research , cell , biochemistry , smooth muscle , immunology , medicine , biology , organic chemistry
Atherosclerosis is a chronic inflammatory disorder of the arteries. Since chronic inflammation increases various adhesion molecules, interfering with the expression of adhesion molecules may be an important therapeutic target of inflammatory disorder. Ramalin has been known to have a variety of biological activities including anti‐inflammatory activity. However, other biological activities of ramalin and its molecular mechanism remain unknown. We examined the effect of ramalin on the expression of the vascular cell adhesion molecule (VCAM‐1) and peptidylarginine deiminase IV (PADI4) in TNF‐α‐induced human aortic smooth muscle cells (HASMCs). Cell adhesion assay and western blotting showed that ramalin dose–dependently inhibited TNF‐α‐induced adhesion of THP‐1 monocytic cells and expression of VCAM‐1 and PADI4. In addition, inhibition of PADI4 activity by siPADI4 suppressed TNF‐α‐induced VCAM‐1 and c‐Fos protein expression, suggesting that PADI4 is involved in VCAM‐1 expression. Our data also revealed that ramalin inhibited phosphorylation of MAPKs and the nuclear translocation of NK‐κB and AP‐1 induced by TNF‐α. Overall, these results provide ramalin inhibits TNF‐α‐induced VCAM‐1 expression through the suppression of PADI4, MAPKs, NF‐κB and AP‐1 signaling pathways and may be considered in therapeutic strategy to reduce the risk of atherosclerosis.